丹酚酸B盐对二甲基亚硝胺诱导的肝纤维化大鼠肝脏转化生长因子β1及其受体蛋白表达的影响
肝纤维化,,],肝纤维化;,丹酚酸B盐;,二甲基亚硝胺;,TGFβ1;,受体,1材料与方法,2结果,3讨论
[摘要] 目的:研究中药丹参的有效成分丹酚酸B盐抗肝纤维化作用的机制。方法:Wistar大鼠24只随机分为正常对照组、模型组和丹酚酸B盐治疗组。采用二甲基亚硝胺诱导大鼠肝纤维化模型,丹酚酸B盐治疗组在造模4周后给予丹酚酸B盐治疗4周。治疗结束后,用盐酸水解法检测全部大鼠肝组织中羟脯氨酸的含量,用Western印迹法检测肝组织Ⅰ型胶原蛋白、转化生长因子β1(transforming growth factorbeta1, TGFβ1)、转化生长因子β受体Ⅰ(transforming growth factorbeta receptor type Ⅰ, TβRⅠ)、转化生长因子β受体Ⅱ(transforming growth factorbeta receptor type Ⅱ, TβRⅡ)蛋白的表达。结果:模型组大鼠肝组织中羟脯氨酸的含量、Ⅰ型胶原蛋白、TGFβ1及其受体TβRⅠ和TβRⅡ蛋白的表达较正常对照组均有显著增加,而丹酚酸B盐治疗组的上述指标与模型组比较则均有不同程度的下降。结论:丹酚酸B盐具有明显的抗肝纤维化作用,其作用机制与抑制TGFβ1及其受体蛋白的表达有关。[关键词] 肝纤维化; 丹酚酸B盐; 二甲基亚硝胺; TGFβ1; 受体
Effects of salvianolic acid B on expressions of TGFβ1 and its receptors in liver of rats with dimethylnitrosamineinduced hepatic fibrosis
WANG XiaoNing, HU YiYang, LIU ChengHai, LIU Ping, ZHU DaYuan
(Institute of Liver Diseases, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China; Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China)
ABSTRACT Objective: To study the therapeutic mechanism of salvianolic acid B (SAB) in treating hepatic fibrosis. Methods: Twentyfour Wistar rats were randomly divided into 3 groups: normal control group, untreated group and SABtreated group. Rats in the untreated and SABtreated groups were injected intraperitoneally with 0.5% dimethylnitrosamine (DMN) for 4 weeks, daily for 3 days each week at a dose of 10 μg/kg, to induce hepatic fibrosis. Then, rats in the SABtreated group were given SAB orally for another 4 weeks. Hydroxyproline (Hyp) contents in liver tissue of the rats in 3 groups were determined with HCl hydrolysis, and collagen typeⅠ, transforming growth factorbeta 1 (TGFβ1), transforming growth factorbeta receptor typeⅠ(TβRⅠ) and transforming growth factorbeta receptor typeⅡ(TβRⅡ) were detected by Western blotting. Results: The Hyp content and the expressions of collagen typeⅠ, TGFβ1, TβRⅠ and TβRⅡ in the liver tissue of rats in the untreated group increased significantly as compared with those in the normal control group, while those in SABtreated group decreased significantly as compared with those in the untreated group. Conclusion: The therapeutic mechanism of SAB in treating hepatic fibrosis may be related to inhibiting the expressions of TGFβ1 and its receptors. ......
您现在查看是摘要页,全文长 10721 字符。